Onset Of Puberty In Females Research Articles

Characterization of the dynamic change of microRNA expression in mice hypothalamus during the time of female puberty

Puberty onset is a milestone in sexual development. A tumor suppress gene (TSG) network had been reported to be involved in the regulation of female puberty onset. The observations in rodents and primates showed a potential link between microRNAs and puberty onset. To figure out what miRNAs play roles in this important biological process, profilings of microRNAs in the hypothalamus of female mice from three different pubertal stages, juvenile [postnatal day (P10)], early pubertal (P25) and pubertal (P30) were performed on the Affymetrix GeneChip miRNA 3.0 Arrays, the cerebral cortex (CTX) was used as a control tissue. 20 miRNAs were shown to be differentially expressed in hypothalamus (fold change > 1.5, P < 0.05), but not in CTX during the transition from juvenile to pubertal. Four of them were validated by real-time quantitative RT-PCR (qRT-PCR) method. 1018 genes were predicted as the targets of these miRNAs. Further bioinformatics analysis suggested that these target genes were involved in many important signaling pathways, especially in the cancer related pathways. We also found that about 90% of these target genes were expressed in the hypothalamus, as well as in the immortalized GnRH-producing GT1-7 cells, which provided additional evidence that these miRNAs could be female puberty onset related. Here we present a novel comprehensive data set of miRNA gene expression during the puberty onset; and it provides an important recourse for the future functional characterization of individual miRNAs and their targets in mouse hypothalamus and in GT1-7 cells.

Determinants of pre-menarcheal knowledge of menstruation and sociocultural implications in college going girls: A community-based cross-sectional study from Latur, Maharashtra

Introduction: Adolescence marks the onset of female puberty. The first menstruation is often horrifying and traumatic to an adolescent girl because it usually occurs without her knowing about it. Implications of a girl's response to menarche have a socio-cultural and religious significance. Aim and Objective: To study the sociocultural and physiological implications of menstruation in college going girls. Materials and Methods: This was a community-based cross-sectional observational study undertaken among college girls. All the girls (n = 252) of the college were enrolled in the study. A structured questionnaire was used as the study tool. The questionnaire included topics related to sociodemographic information, sociocultural implications and first informant about the physiological process of menstruation along with its timing. Results: Majority of the study subjects (77.40%) observed restrictions for religious/holy things. Sleep disturbances were the most common (59%) disturbance faced by the study subjects. Of a total of 252 respondents, majority [104 (41.30%)] had leg cramps. The first informant of menstruation was the mother in 196 (77.78%) girls. Of 252 girls, 86 (34.12%) had pre-menarcheal knowledge of menstruation. Mothers from the urban area and with better education tend to give knowledge of menstruation prior to menarche of her daughter. An increasing trend was observed with increasing educational status of the mother and proportion of them giving pre-menarcheal knowledge of menstruation to their daughter. Conclusions: Menstruation is associated with a high burden of sociocultural implications. Pre-menarcheal knowledge of menstruation is poor. Mothers from the urban area and with better educational level tend to give knowledge of menstruation prior to menarche of their daughter.

Co-education with environmental cues may kindle early onset of female puberty

Co-education with environmental cues may kindle early onset of female puberty

Delay of the onset of puberty in female rats by prepubertal exposure to T-2 toxin.

Growing evidence has revealed the deleterious influence of environmental and food contaminants on puberty onset and development in both animals and children, provoking an increasing health concern. T-2 toxin, a naturally-produced Type A trichothecene mycotoxin which is frequently found in cereal grains and products intended for human and animal consumption, has been shown to impair the reproduction and development in animals. Nevertheless, whether this trichothecene mycotoxin can disturb the onset of puberty in females remains unclear. To clarify this point, infantile female rats were given a daily intragastric administration of vehicle or 187.5 μg/kg body weight of T-2 toxin for five consecutive days from postnatal day 15 to 19, and the effects on puberty onset were evaluated in the present study. The results revealed that the days of vaginal opening, first dioestrus, and first estrus in regular estrous cycle were delayed following prepubertal exposure to T-2 toxin. The relative weights of reproductive organs uterus, ovaries, and vagina, and the incidence of corpora lutea were all diminished in T-2 toxin-treated rats. Serum levels of gonadotropins luteinizing hormone, follicle-stimulating hormone, and estradiol were also reduced by T-2 toxin treatment. The mRNA expressions of hypothalamic gonadotropin-releasing hormone (GnRH) and pituitary GnRH receptor displayed significant reductions following exposure to T-2 toxin, which were consistent with the changes of serum gonadotropins, delayed reproductive organ development, and delayed vaginal opening. In conclusion, the present study reveals that prepubertal exposure to T-2 toxin delays the onset of puberty in immature female rats, probably by the mechanism of disturbance of hypothalamic-pituitary-gonadal (HPG) axis function. Considering the vulnerability of developmental children to food contaminants and the relative high level of dietary intake of T-2 toxin in children, we think the findings of the present study provide valuable information for the health risk assessment in children.

Disruption of Zebrafish Follicle-Stimulating Hormone Receptor (fshr) But Not Luteinizing Hormone Receptor (lhcgr) Gene by TALEN Leads to Failed Follicle Activation in Females Followed by Sexual Reversal to Males.

Gonadotropins are primary hormones that control vertebrate reproduction. In a recent study, we analyzed the impacts of FSH and LH on zebrafish reproduction by disrupting FSH and LH-β genes (fshb and lhb) using transcription activator-like effector nuclease (TALEN) technology. Using the same approach, we successfully deleted FSH and LH receptor genes (fshr and lhcgr) in the present study. In contrast to the deficiency of its cognate ligand FSH, the fshr-deficient females showed a complete failure of follicle activation with all ovarian follicles arrested at the primary growth-previtellogenic transition, which is the marker for puberty onset in females. Interestingly, after blockade at the primary growth stage for varying times, all females reversed to males, and all these males were fertile. In fshr-deficient males, spermatogenesis was normal in adults, but the initiation of spermatogenesis in juveniles was retarded. In contrast to fshr, the deletion of the lhcgr gene alone caused no obvious phenotypes in both males and females; however, double mutation of fshr and lhcgr resulted in infertile males. In summary, our results in the present study showed that Fshr was indispensable to folliculogenesis and the disruption of the fshr gene resulted in a complete failure of follicle activation followed by masculinization into males. In contrast, lhcgr does not seem to be essential to zebrafish reproduction in both males and females. Neither Fshr nor Lhcgr deficiency could phenocopy the deficiency of their cognate ligands FSH and LH, which is likely due to the fact that Fshr can be activated by both FSH and LH in the zebrafish.

Phenotype-genotype correlations in 17 new patients with an Xp11.23p11.22 microduplication and review of the literature.

Array comparative genomic hybridization (array CGH) has proven its utility in uncovering cryptic rearrangements in patients with X-linked intellectual disability. In 2009, Giorda et al. identified inherited and de novo recurrent Xp11.23p11.22 microduplications in two males and six females from a wide cohort of patients presenting with syndromic intellectual disability. To date, 14 females and 5 males with an overlapping microduplication have been reported in the literature. To further characterize this emerging syndrome, we collected clinical and microarray data from 17 new patients, 10 females, and 7 males. The Xp11.23p11.2 microduplications detected by array CGH ranged in size from 331 Kb to 8.9 Mb. Five patients harbored 4.5 Mb recurrent duplications mediated by non-allelic homologous recombination between segmental duplications and 12 harbored atypical duplications. The chromosomal rearrangement occurred de novo in eight patients and was inherited in six affected males from three families. Patients shared several common major characteristics including moderate to severe intellectual disability, early onset of puberty, language impairment, and age related epileptic syndromes such as West syndrome and focal epilepsy with activation during sleep evolving in some patients to continuous spikes-and-waves during slow sleep. Atypical microduplications allowed us to identify minimal critical regions that might be responsible for specific clinical findings of the syndrome and to suggest possible candidate genes: FTSJ1 and SHROOM4 for intellectual disability along with PQBP1 and SLC35A2 for epilepsy. Xp11.23p11.22 microduplication is a recently-recognized syndrome associated with intellectual disability, epilepsy, and early onset of puberty in females. In this study, we propose several genes that could contribute to the phenotype.

Feeding prepubescent gilts a high-fat diet induces molecular changes in the hypothalamus-pituitary-gonadal axis and predicts early timing of puberty

ObjectiveThe onset of puberty in females has been occurring earlier over the past decades, presumably as a result of improved nutrition in developed countries. However, the underlying molecular mechanisms responsible for the early attainment of puberty as a result of nutrition fortification remain largely unknown. The aim of this study was to evaluate the hormone and gene expression changes in prepubescent gilts fed a high-fat diet to investigate whether these changes could predict the early timing of puberty. MethodsForty gilts were fed a daily basal diet (LE) or a basal diet with an additional 270 g/d or 340 g/d of fat (HE) during the prepubescent phase. Blood samples were collected during the prepubescent phase to detect hormone secretion changes in insulin-like growth factor-1, kisspeptin, estradiol, progesterone, and leptin. The gene expressions at the hypothalamus–pituitary–gonadal axis were examined on day 73 of the experiment (average age on day 177) during the prepubescent phase. ResultsAn HE diet resulted in accelerated body weight gain and back-fat thickness at the P2 point compared with LE gilts during the prepubescent phase. Gilts that were fed HE diets attained puberty 12 d earlier than LE gilts, and a larger proportion of HE gilts reached puberty at day 180 or 190 of age. A postmortem analysis revealed a promoted development of the uterus and ovary tissue that was characterized by a 53.7% and 29.5% increase in the uterine and ovary weight, respectively, and an increased length of the uterine horn and oviduct tissue in HE gilts. Real-time quantitative polymerase chain reaction revealed that HE gilts had higher Kiss-1, G protein-coupled receptor 54, gonadotropin-releasing hormone and estrogen receptor α mRNA expression levels in the hypothalamic anteroventral periventricular nucleus; the leptin receptor mRNA expression level was higher in the hypothalamic arcuate nucleus and ovary tissue; the insulin-like growth factor-1 receptor expression was higher in the pituitary and ovary tissues, and the follicle-stimulating hormone and luteinizing hormone mRNA expression levels were higher in the pituitary gland. ConclusionThese data showed that the consumption of additional fat can facilitate early attainment of puberty, which can be predicted by the changes in secreted hormones and gene expression in the hypothalamus-pituitary-gonadal axis.

Genetic dissection of puberty in mice

Determining the neural mechanisms controlling gonadotrophin-releasing hormone (GnRH) release is of pivotal importance in understanding central control of reproductive physiology in vertebrates. Targeted genetic manipulation of kisspeptin and GPR54 neurons has provided new insights into the mechanisms modulating GnRH release and thereby regulating hypothalamic-pituitary-gonadal axis activity during reproductive maturation. While conditional ablation of the oestrogen receptor α gene in kisspeptin neurons results in a dramatic advancement of the onset of puberty in female mice, subsequent pubertal maturation is arrested in these animals, as they fail to acquire normal ovulatory cyclicity. These data suggest that two oestrogen receptor α-dependent mechanisms, one a 'brake' and the other an 'accelerator', are sequentially operated in kisspeptin neurons during pubertal development of female mice to gate and then to activate GnRH release. In a different experimental approach, we removed entire kisspeptin neurons from the mouse brain and thus from the neural circuits controlling reproduction. Surprisingly, the onset of puberty in females was unaffected by kisspeptin neuron ablation. Furthermore, the animals attained regular ovulatory cyclicity and were fertile. Consistent with this, female mice lacking neurons that express the kisspeptin receptor GPR54 were also fertile, suggesting female reproductive maturation in the absence of kisspeptin/GPR54 signalling. However, acute kisspeptin neuron ablation in adult mice inhibited fertility, indicating that there is developmental compensation for the loss of kisspeptin neurons during reproductive neural circuit formation. Finally, we showed that kisspeptin neurons become an indispensable part of reproductive neural circuitry in the mouse brain before postnatal day 20.

Metabolic Programming of Puberty: Sexually Dimorphic Responses to Early Nutritional Challenges

Body energy stores and metabolic cues influence the onset of puberty. However, the pubertal impact of early nutritional challenges has been only fragmentarily addressed. We evaluated here the consequences, in terms of pubertal timing and hormonal markers, of various nutritional manipulations during pre- or postnatal maturation in rats of both sexes. Males and females were submitted to gestational undernutrition (UNG) or peripubertal (SUB) subnutrition or were raised in large (LL; underfeeding) or small (SL; overfeeding) litters. In addition, groups of UNG, LL, and SL rats were fed on a high-fat diet (HFD) after weaning. Postnatal overfeeding resulted in higher body weights (BWs) during pubertal transition in both sexes, but only SL males displayed overtly advanced external signs of puberty. Postnatal underfeeding persistently decreased BW gain during puberty, yet the magnitude of pubertal delay was greater in LL males. In contrast, regardless of postnatal nutrition, HFD tended to advance the onset of puberty in females but did not alter pubertal timing in males. Likewise, SUB females displayed a marked delay in BW gain and puberty onset, whereas despite similar reduction in BW, SUB males showed normal timing of puberty. These sex divergences were also detected in various hormonal and metabolic indices so that postnatal overnutrition consistently increased LH, FSH, leptin, and insulin levels only in pubertal females, whereas HFD decreased gonadotropin levels in SL females but increased them in SL males. Notably, UNG rats did not show signs of delayed puberty but displayed a striking sex dimorphism in serum insulin/glucose levels, regardless of the diet, so that only UNG males had signs of presumable insulin resistance. Our data disclose important sex differences in the impact of various early nutritional challenges on the timing of puberty, which may help to explain the different trends of altered puberty and related comorbidities between sexes.

A piece in the puzzle of puberty

The onset of puberty in mammals is determined by a poorly understood mix of genetics and environment. A survey of the epigenetic methylation landscape provides insight into a potential mechanism for the onset of puberty in females involving emancipation from a repressive gene complex in hypothalamic neurons.

Prenatal Exposure to Low Levels of Androgen Accelerates Female Puberty Onset and Reproductive Senescence in Mice

Sex steroid hormone production and feedback mechanisms are critical components of the hypothalamic-pituitary-gonadal (HPG) axis and regulate fetal development, puberty, fertility, and menopause. In female mammals, developmental exposure to excess androgens alters the development of the HPG axis and has pathophysiological effects on adult reproductive function. This study presents an in-depth reproductive analysis of a murine model of prenatal androgenization (PNA) in which females are exposed to a low dose of dihydrotestosterone during late prenatal development on embryonic d 16.5-18.5. We determined that PNA females had advanced pubertal onset and a delay in the time to first litter, compared with vehicle-treated controls. The PNA mice also had elevated testosterone, irregular estrous cyclicity, and advanced reproductive senescence. To assess the importance of the window of androgen exposure, dihydrotestosterone was administered to a separate cohort of female mice on postnatal d 21-23 [prepubertal androgenization (PPA)]. PPA significantly advanced the timing of pubertal onset, as observed by age of the vaginal opening, yet had no effects on testosterone or estrous cycling in adulthood. The absence of kisspeptin receptor in Kiss1r-null mice did not change the acceleration of puberty by the PNA and PPA paradigms, indicating that kisspeptin signaling is not required for androgens to advance puberty. Thus, prenatal, but not prepubertal, exposure to low levels of androgens disrupts normal reproductive function throughout life from puberty to reproductive senescence.

Regulation of the female rat estrous cycle by a neural cell-specific epidermal growth factor-like repeat domain containing protein, NELL2.

NELL2, a protein containing epidermal growth factor-like repeat domains, is predominantly expressed in the nervous system. In the mammalian brain, NELL2 expression is mostly neuronal. Previously we found that NELL2 is involved in the onset of female puberty by regulating the release of gonadotropin-releasing hormone (GnRH), and in normal male sexual behavior by controlling the development of the sexually dimorphic nucleus of the preoptic area (POA). In this study we investigated the effect of NELL2 on the female rat estrous cycle. NELL2 expression in the POA was highest during the proestrous phase. NELL2 mRNA levels in the POA were increased by estrogen treatment in ovariectomized female rats. Blocking NELL2 synthesis in the female rat hypothalamus decreased the expression of kisspeptin 1, an important regulator of the GnRH neuronal apparatus, and resulted in disruption of the estrous cycle at the diestrous phase. These results indicate that NELL2 is involved in the maintenance of the normal female reproductive cycle in mammals.

Female reproductive maturation in the absence of kisspeptin/GPR54 signaling

Puberty onset is initiated in the brain by activation of gonadotropin-releasing hormone (GnRH) neurosecretion. Different permissive signals must be integrated for the initiation of reproductive maturation; however, the neural circuits controlling timely awakening of the reproductive axis are not understood. The identification of the neuropeptide kisspeptin as a potent activator of GnRH neuronal activity suggests that kisspeptin-releasing neurons might coordinate puberty onset. To test this hypothesis, we generated mice that specifically lack kisspeptin cells. Puberty onset in females was unaffected by kisspeptin neuron ablation. Furthermore, the animals were fertile, albeit with smaller ovaries. Consistent with this, female mice lacking neurons that express the kisspeptin receptor GPR54 were also fertile. Acute ablation of kisspeptin neurons in adult mice inhibited fertility, suggesting that there is compensation for the loss of kisspeptin neurons early in development. Our data indicate that the initiation and completion of reproductive maturation can occur in the absence of kisspeptin/GPR54 signaling.

Analysis of Male Pheromones That Accelerate Female Reproductive Organ Development

Male odors can influence a female's reproductive physiology. In the mouse, the odor of male urine results in an early onset of female puberty. Several volatile and protein pheromones have previously been reported to each account for this bioactivity. Here we bioassay inbred BALB/cJ females to study pheromone-accelerated uterine growth, a developmental hallmark of puberty. We evaluate the response of wild-type and mutant mice lacking a specialized sensory transduction channel, TrpC2, and find TrpC2 function to be necessary for pheromone-mediated uterine growth. We analyze the relative effectiveness of pheromones previously identified to accelerate puberty through direct bioassay and find none to significantly accelerate uterine growth in BALB/cJ females. Complementary to this analysis, we have devised a strategy of partial purification of the uterine growth bioactivity from male urine and applied it to purify bioactivity from three different laboratory strains. The biochemical characteristics of the active fraction of all three strains are inconsistent with that of previously known pheromones. When directly analyzed, we are unable to detect previously known pheromones in urine fractions that generate uterine growth. Our analysis indicates that pheromones emitted by males to advance female puberty remain to be identified.

Onset of puberty and early-life reproduction in Angus females divergently selected for post-weaning residual feed intake

Angus cattle that had been divergently selected for Low and High post-weaning residual feed intake (RFI) were used in two projects to evaluate early-life reproductive performance and onset of puberty in females. In the first project, data on the 1999-born females (n = 64) were evaluated for weight, subcutaneous fat (P8 fat depth) and reproductive performance over two breeding cycles. These females that were the result of 1.0–2.5 (mean of 1.8) generations of selection, had mean (±s.e.) post-weaning RFI of –0.82 ± 0.19 kg/day and 0.57 ± 0.18 kg/day for the Low and High RFI selection lines, respectively. In the second project, ultrasonography was used to scan the ovaries of the 2008-born heifers (n = 121) on four occasions following weaning. In these heifers the presence of corpus luteum provided evidence of ovulation, and hence the commencement of onset of puberty. The average of the estimated breeding value (EBV) for RFI of the parents of the Low RFI and the High RFI selection line heifers were –0.72 ± 0.05 and 0.37 ± 0.03 kg/day, respectively. In the first project, no significant selection line differences were evident for weight, age at first mating, pregnancy and calving rates (percentage of females that were pregnant, or the percentage that calved out of the total number used for mating), calf birthweight and weight of calf born per female exposed to bull. Females from the Low RFI line had significantly (P &lt; 0.05) lower P8 fat depth relative to their High RFI contemporaries at most of the measurement dates (e.g. 9.2 ± 0.5 versus 12.0 ± 0.5 mm at the start of first mating). Low RFI females also calved significantly (P &lt; 0.05) later in the calving season than High RFI females (35.7 ± 3.0 versus 27.6 ± 2.4 days). The results indicate that there is a delayed pregnancy date during the first mating season leading to a later calving date for the Low RFI heifers. The later first calving date was then maintained at subsequent calving. The later calving, however, did not impact on pregnancy and calving rates. In the second project, it was observed that irrespective of selection line, heifers that had attained onset of puberty had significantly (P &lt; 0.05) greater P8 fat depth than those that had not. Hence the expectation was that, relative to High RFI heifers, the Low RFI heifers with their lower P8 fat, will attain onset of puberty at a slightly older age. This expected trend was observed but the difference was not significant, and further investigations are recommended.

Neuroendocrine, Metabolic and Genomic Cues Signalling the Onset of Puberty in Females

ContentsPuberty is the result of a dynamic interaction between genetic factors and environmental cues, all of which lead to the attainment of reproductive capacity. Thus, significant changes in hormone secretion occur from the pre‐pubertal to the pubertal stage. The objective of this review is to provide an update of some endocrine, physiological, metabolic and genetic concepts involved in the establishment of the hypothalamic‐hypophyseal‐gonadal axis function promoting the onset of the reproductive function during puberty. To achieve this purpose, basic aspects of the function of the hypothalamic‐hypophyseal‐gonadal axis, the control of the axis by neurotransmitters and the interaction between reproductive function and metabolic status will be considered. Finally, the role of the novel kisspeptin system and the GPR54 receptor as modulators of puberty will be considered, in addition to the hierarchical expression of the main genes acting as regulators of the onset of puberty.

Chronic treatment with polychlorinated biphenyls (PCB) during pregnancy and lactation in the rat: Part 2: Effects on reproductive parameters, on sex behavior, on memory retention and on hypothalamic expression of aromatase and 5alpha-reductases in the offspring

The gender-specific expression pattern of aromatase and 5alpha-reductases (5alpha-R) during brain development provides neurons the right amount of estradiol and DHT to induce a dimorphic organization of the structure. Polychlorinated biphenyls (PCBs) are endocrine disruptive pollutants; exposure to PCBs through placental transfer and breast-feeding may adversely affect the organizational action of sex steroid, resulting in long-term alteration of reproductive neuroendocrinology. The study was aimed at: a) evaluating the hypothalamic expression of aromatase, 5alpha-R1 and 5alpha-R2 in fetuses (GD20), infant (PN12), weaning (PN21) and young adult (PN60) male and female rats exposed to PCBs during development; b) correlating these parameters with the time of testicular descent, puberty onset, estrous cyclicity and copulatory behavior; c) evaluating possible alterations of some non reproductive behaviors (locomotion, learning and memory, depression/anxiety behavior). A reconstituted mixture of four indicator congeners (PCB 126, 138, 153 and 180) was injected subcutaneously to dams at the dose of 10 mg/kg daily from GD15 to GD19 and then twice a week till weanling. The results indicated that developmental PCB exposure produced important changes in the dimorphic hypothalamic expression of both aromatase and the 5alpha-Rs, which were still evident in adult animals. We observed that female puberty onset occurs earlier than in control animals without cycle irregularity, while testicular descent in males was delayed. A slight but significant impairment of sexual behavior and an important alteration in memory retention were also noted specifically in males. We conclude that PCBs might affect the dimorphic neuroendocrine control of reproductive system and of other neurobiological processes.

Delayed Puberty in Spontaneously Hypertensive Rats Involves a Primary Ovarian Failure Independent of the Hypothalamic KiSS-1/GPR54/GnRH System

Spontaneously hypertensive (SH) rats, extensively used as experimental models of essential human hypertension, display important alterations in the neuroendocrine reproductive axis, which manifest as markedly delayed puberty onset in females but whose basis remains largely unknown. We analyze herein in female SH rats: 1) possible alterations in the expression and function of KiSS-1/GPR54 and GnRH/GnRH-receptor systems, 2) the integrity of feedback mechanisms governing the hypothalamic-pituitary-ovarian axis, and 3) the control of ovarian function by gonadotropins. Our data demonstrate that, despite overtly delayed puberty, no significant decrease in hypothalamic KiSS-1, GPR54, or GnRH mRNA levels was detected in this strain. Likewise, in vivo gonadotropin responses to ovariectomy and systemic kisspeptin-10 or GnRH administration, as well as in vitro gonadotropin responses to GnRH, were fully preserved in SH rats. Moreover, circulating LH levels were grossly conserved during prepubertal maturation, whereas FSH levels were even enhanced from d 20 postpartum onwards. In striking contrast, ovarian weight and hormone (progesterone and testosterone) responses to human chorionic gonadotropin (CG) in vitro were profoundly decreased in SH rats, with impaired follicular development and delayed ovulation at puberty. Such reduced hormonal responses to human CG could not be attributed to changes in LH/CG or FSH-receptor mRNA expression but might be linked to blunted P450scc, 3beta-hydroxy steroid dehydrogenase, and aromatase mRNA levels in ovaries from SH rats. In conclusion, our results indicate that the expression and function of KiSS-1/GPR54 and GnRH/GnRH-receptor systems is normal in SH rats, whereas ovarian development, steroidogenesis, and responsiveness to gonadotropins are strongly compromised.

Organizational effects of DDE on brain vasotocin system in male Japanese quail

p,p′-DDE, or ethylene, 1,1-dichloro-2,2-bis(p-chlorophenyl), is the main metabolite of the pesticide DDT, or 1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane. It is an androgen receptor antagonist and testosterone hydroxylase modulator that is also more persistent than its parent compound. In a previous study we demonstrated that embryonic exposure to different doses of p,p′-DDE accelerated onset of puberty in females and reduced male reproductive behavior. In the present study we investigated the long-term effects of the exposure to p,p′-DDE on the differentiation of male Japanese quail ( Coturnix japonica) limbic circuits related to male copulatory behavior: the parvocellular vasotocin (VT) system. We observed a decrease in the density of VT-immunoreactive fibers within the medial preoptic nucleus, bed nucleus of the stria terminalis, and lateral septum in p,p′-DDE-treated birds, while no differences could be detected in the magnocellular neurons of the supraoptic nucleus. In particular the lowest dose of p,p′-DDE causes the highest decrease of VT immunoreactivity. This study provides further evidence for VT system sensitivity towards endocrine disrupting chemicals and demonstrates that the VT system may be an appropriate and sensitive biomarker for early p,p′-DDE exposure in birds.

The stimulatory effect of male agouti (Dasyprocta prymnolopha) on the onset of female puberty

The objective of this research was to analyze female agouti puberty. We did not observe the onset of puberty when the females were raised without males. When an adult male was put together with other adults and no cycling females, the onset of estrous cycle was observed after 10 to 60 days. When the young females were raised with a male, the onset of puberty was reached at 9 months. We concluded that the male agouti influences the onset of puberty in females, and that the dominant female, apparently, inhibits or delays the puberty of the other agouti females of the group. We suggest further studies be made concerning the social control of the reproduction of these animal.